Evidence map›Paper›PMID 25446898›Full record

ArticleCancer cell2014

Cells of origin in the embryonic nerve roots for NF1-associated plexiform neurofibroma.

Zhiguo Chen, Chiachi Liu, Amish J Patel, Chung-Ping Liao, Yong Wang, Lu Q Le

Open access · bronzeAbstract read
In one paragraph

Article in Cancer cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
4.9field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

67 citing papers in PubMed, 100 citations in OpenAlex.

  1. Review
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  9. Biomedicines · 2024
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  11. TheCancers · 2024
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  14. Combined CDK4/6 and ERK1/2 Inhibition Enhances Antitumor Activity in NF1-Associated Plexiform Neurofibroma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  15. Review
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7 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Zhiguo ChenDepartment of Dermatology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9133, USA.
Chiachi LiuDepartment of Dermatology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9133, USA.
Amish J PatelDepartment of Dermatology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9133, USA; Cancer Biology Graduate Program, University of Texas Southwestern Medical Center, Dallas, TX 75390-9133, USA.
Chung-Ping LiaoDepartment of Dermatology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9133, USA.
Yong WangDepartment of Dermatology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9133, USA.
Lu Q LeDepartment of Dermatology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9133, USA; Harold C. Simmons Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75390-9133, USA; UTSW Neurofibromatosis Clinic, University of Texas Southwestern Medical Center, Dallas, TX 75390-9133, USA. Electronic address: lu.le@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · USSouthwestern Medical Center · US

Funding

Transcriptional Function of Krox20 in Development and TumorigenesisR01CA166593 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI LE, LU · 2012 to 2022
$3.7M
NCI NIH HHS R01 CA166593
6 · The paper itself

Abstract

Neurofibromatosis type 1 is a tumor-predisposing genetic disorder. Plexiform neurofibromas are common NF1 tumors carrying a risk of malignant transformation, which is typically fatal. Little is known about mechanisms mediating initiation and identity of specific cell type that gives rise to neurofibromas. Using cell-lineage tracing, we identify a population of GAP43(+) PLP(+) precursors in embryonic nerve roots as the cells of origin for these tumors and report a non-germline neurofibroma model for preclinical drug screening to identify effective therapies. The identity of the tumor cell of origin and facility for isolation and expansion provides fertile ground for continued analysis to define factors critical for neurofibromagenesis. It also provides unique approaches to develop therapies to prevent neurofibroma formation in NF1 patients.

Indexed as

AnimalsCarcinogenesisCell LineageDisease Models, AnimalEmbryo, MammalianFemaleGanglia, SpinalGAP-43 ProteinMice, TransgenicMyelin Proteolipid ProteinNeurofibroma, PlexiformNeurofibromin 1Peripheral Nervous System NeoplasmsGAP-43 ProteinMyelin Proteolipid ProteinNeurofibromin 1Plp1 protein, mouse

Identifiers

PMID25446898
PMCPMC4254535
OpenAlexW2069255325

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.